The first known case of neutrophilic arterial vasculitis was reported in a patient with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, according to a letter to the editor published in Rheumatology. Based on a multidisciplinary discussion with hematologists, rheumatologists, pneumologists, and nephrologists, the report explores a novel and significant manifestation of coronavirus disease 2019 (COVID-19).
A 73-year-old man with a history of type 2 diabetes, chronic kidney disease (CKD), and ischemic coronary disease was admitted to a hospital in Italy with dry cough and shortness of breath. An oropharyngeal swab tested positive for SARS-CoV-2. The patient was initiated with antithrombotic prophylaxis with low-molecular-weight heparin (LMWH; 4000 U/d) and continued to receive therapy with acetylsalicylic acid (100 mg/d). However, the patient presented with an acute abdomen, the day after hospital admission. Scans revealed arterial multifocal thrombosis; the patient then underwent splenectomy and resection of the ischemic bowel loop. After surgery, the patient showed characteristics of an acute exacerbation of CKD, which required hemodialysis.
A total of 16 days after the initial COVID-19 test, the patient was tested negative for SARS-CoV-2. However, 60 days after admission, the patient remained hospitalized largely due to post-surgical complications. The patient did not receive immunosuppressive therapy or mechanical ventilation. The histopathologic diagnosis was neutrophilic vasculitis, with no SARS-CoV-2 on splenic artery wall specimens. Authors of the letter discussed the implications of these complications from various specialist perspectives.
Studies have suggested that some patients with severe COVID-19 may meet the criteria for sepsis-induced coagulopathy. From a hematologist perspective, the patient improved after anticoagulant therapy, supporting its potential role in treating severe COVID-19 manifestations.
Rheumatologists noted case similarities to the acute stage of polyarteritis nodosa (PAN). As with PAN, the patient in this case study presented with gastrointestinal and splenic involvement with ischemic complications. However, his condition improved without immunosuppressive treatment while he was receiving anticoagulant therapy, which is typically indicated in thrombotic complications of PAN.
Lung involvement in COVID-19 has been reported to enhance local inflammation and promote pulmonary vascular microthrombosis. Pneumologists suggested that pulmonary vasculitis may have enhanced lung damage and not affected compliance in the patient. They noted that this pathology mimicked that of interstitial lung disorders, which may explain the patient’s presentation with shortness of breath despite lack of respiratory failure.
Nephrologists included in the study suggested that the patient’s severe acute kidney injury may have been secondary to COVID-19. Further, while abdominal surgery could have resulted in kidney complications, the partial recovery of kidney function with immunosuppressive therapy may suggest a link to COVID-19. However, without a biopsy, a direct relationship cannot be confirmed.
This case study represents early efforts to characterize unique and serious manifestations of COVID-19. Further monitoring of thrombotic complications in these patients is essential to determining appropriate care routes.
The main limitation of the analysis was the scarce availability of diagnostic procedures.
“[I]t is conceivable to attribute a leading role to anticoagulant treatments in the management of COVID-19,” authors of the letter concluded. “Nevertheless, while primary LMWH may be effective in the prevention of endothelial activation-induced thrombosis, this might not be the case when thrombotic phenomena are secondary to vasculitis, which could benefit from immunosuppressive therapy.”
Vacchi C, Meschiari M, Milic J, et al. COVID-19-associated vasculitis and thrombotic complications: from pathological findings to multidisciplinary discussion. Letter. Rheumatology (Oxford). Published September 24, 2020. doi:10.1093/rheumatology/keaa581